Cardiac cycles are divided into two parts—systole and diastole. During systole, the ventricles (the heart's major pumping chambers) contract, thus ejecting blood out of the heart and into the arteries. After the ventricles have finished contracting, they relax, and during a portion of this relaxation phase they re-fill with blood to prepare for the next contraction. This relaxation phase is called diastole. More specifically, diastole is the phase of a cardiac cycle when the ventricles are not contracting, but rather are relaxed and filling with blood that is being returned, either from the body (into right ventricle) or from the lungs (into left ventricle).
With reference to the left side of the heart, blood flows from the lungs, into the pulmonary veins, into the left atrium, past the mitral valve, and finally into the left ventricle. When the left ventricle cannot fill adequately during diastole, blood will accumulate in the left atrium and, eventually, in the lungs. The result is a higher than normal pressure of blood within the vessels of the lung. As a result of hydrostatic forces, this high pressure leads to leaking of fluid (i.e. transudate) from the lung's blood vessels into the air-spaces (alveoli) of the lungs. This can result in pulmonary edema, a condition characterized by difficult breathing, inadequate oxygenation of blood, and, if severe and untreated, death.
Diastolic function, which refers the function of the ventricles during diastole, is a useful measure for monitoring a patient's cardiac health. An abnormal diastolic function, which is referred to as diastolic dysfunction, is characterized by elevated diastolic pressure in the left ventricle despite normal or sub-normal diastolic volume. Hypertrophy of cardiac cells, increased interstitial collagen deposition or infiltration of the myocardium with amyloid proteins causes decreased distensibility of the cardiac tissue. The ventricle then behaves as a balloon made from abnormally thick rubber. Despite filling with high pressure, the volume cannot expand adequately. If the heart cannot fill with blood easily, either the cardiac output becomes diminished or compensation ensues to increase the ventricular diastolic pressure to higher levels. When the left ventricular diastolic pressure is elevated, venous pressure in the lungs must also become elevated to maintain forward flow. Increased pulmonary venous pressure results in alveolar edema causing the patient to be short of breath.
Useful measures of diastolic function include measures of a patient's ventricular diastolic period (also referred to simply as the diastolic period), which is the duration of diastole in a single cardiac cycle. Useful measures of diastolic function also include isovolumic relaxation time (IVRT) and left ventricular diastolic filling time (DiFT), which together make up the diastolic period (DP). The diastolic period starts at closure of the aortic valve and ends at closure of the mitral valve. The IVRT, which starts at closure of the aortic valve and ends at opening of the mitral valve, is the portion of the diastolic period during which the left ventricular muscle decreases its tension without lengthening so that left ventricular volume remains unaltered. The DiFT, which starts at opening of the mitral valve and ends at closing of the mitral valve, is the total amount of time during which the left ventricle becomes filled with blood during diastole. DP, IVRT and DiFT are typically measured using an echocardiogram (ECHO), which can not be chronically obtained, and can not be obtained by an implantable system. Accordingly, there is still a need for systems and methods for chronically monitoring diastolic function and heart failure.
Even though the heart may have sufficient systolic pump function to expel much of the blood that fills it each cardiac cycle, diastolic dysfunction may lead to inadequate filling. When diastolic dysfunction becomes severe, diastolic heart failure, or more generally heart failure, can occur. Heart failure (HF) relates to the inability of the heart to maintain adequate circulation of blood in the tissues. Typically the left ventricle cannot pump out sufficient oxygenated blood returned from the lungs. As a result, blood and fluids may begin to accumulate in the lungs, abdomen or legs.
HF patients require close medical management, typically involving multiple pharmacological therapies, to handle this chronic disease with numerous comorbidities. Because the disease status evolves with time, frequent physician follow-up examinations are often necessary. At follow-up, the physician may make adjustments to the drug regimen in order to optimize therapy. This conventional approach of periodic follow-up may be less satisfactory for HF, in which acute, life-threatening exacerbations can develop between physician follow-up examinations. It is well known among clinicians that if a developing exacerbation is recognized early, it can be more easily and inexpensively terminated, typically with a modest increase in oral diuretic. However, if it develops beyond the initial phase, an acute HF exacerbation becomes difficult to control and terminate. Hospitalization in an intensive care unit is often required. During acute exacerbation of heart failure, many patients develop complications, leading to increasing morbidity and mortality. Identification of evolving disease progression may also allow for device therapies, such as pacing therapy from an implanted pulse generator.